MiR-152-3p Affects the Progression of Colon Cancer via the KLF4/IFITM3 Axis. (1st September 2020)

• Record Type: Journal Article
• Authors: Zhu, Xiaoyi; Shen, Zhan; Man, Da; Ruan, Hang; Huang, Sha
• Other Names: Huang Tao Academic Editor.
• Is Part Of: Computational and mathematical methods in medicine. Volume 2020(2020)
• Publication Date: 2020-09-01
• Subjects: Medicine -- Computer simulation -- Periodicals; Medicine -- Mathematical models -- Periodicals; 610.11
• DOI: 10.1155/2020/8209504
• Languages: English
• ISSNs: 1748-670X

Abstract

Abstract : Objective . The purpose of this study was to investigate the relationship between miR-152-3p and the KLF4/IFITM3 axis, thereby revealing the mechanism underlying colon cancer occurrence and development, consequently providing a promising target for colon cancer treatment. Methods . Bioinformatics methods were implemented to analyze the differential expression of miRNAs and mRNAs in colon cancer, confirm the target miRNA, and predict the downstream targeted mRNAs. qRT-PCR and Western blot were performed to detect the expression of miR-152-3p, KLF4, and IFITM3. CCK-8 and colony formation assays were conducted for the assessment of cell proliferation, and flow cytometry was carried out for the detection of cell apoptosis. Finally, dual-luciferase reporter gene assay was employed to verify the targeting relationship between miR-152-3p and KLF4. Results . miR-152-3p was highly expressed in colon cancer cells, whereas KLF4 was poorly expressed. Dual-luciferase assay verified that miR-152-3p targeted to bind to KLF4 and suppressed its expression. Moreover, silencing miR-152-3p or overexpressing KLF4 was found to downregulate IFITM3, thereby inhibiting cell proliferation and potentiating cell apoptosis. In rescue experiments, we found that miR-152-3p deficiency decreased the expression of IFITM3 and weakened cancer cell proliferation, and such effects were restored when miR-152-3p and KLF4 were silenced simultaneously. Conclusion . In sum, we discovered that miR-152-3p can affect the pathogenesis of colon cancer via the KLF4/IFITM3 axis.